Structural responses to voltage-clamping in the toad urinary bladder. II. Granular cells and the natriferic action of vasopressin.
The natriferic action of vasopressin has been investigated with morphological studies of voltage-clamped toad urinary bladders. Granular cell swelling can be induced in the presence of isoosmotic solutions when the orientation of the transmural potential is reversed by voltage clamping (V.A. Bobrycki, J. W. Mills, A.D.C. Macknight & D. R. DiBona, J. Membrane Biol., 60:21, 1981) and results from an increased rate of sodium entry across the mucosal membrane; under these conditions the active transport mechanism at the basal-lateral membrane becomes rate-limiting. Vasopressin exacerbated the voltage-reversal-induced swelling of granular cells while other cell types were unaffected. Granular cell swelling appeared to be dependent upon sodium entry from the mucosal medium since it was completely prevented by amiloride. There was no evidence for an effect of vasopressin on tight junction permeability; voltage-reversal induced the same amount of junction blistering whether or not vasopressin was present. It is concluded that the predominant effect of vasopressin on transepithelial sodium transport is to increase the sodium conductance of the mucosal plasma membrane. As is the case with the hydroosmotic effect of the hormone, the natriferic action of vasopressin seems to be exerted primarily, if not entirely, on the granular cells.
D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002024:Bufo marinus; D002462:Cell Membrane / Q000378:metabolism; D004848:Epithelium / Q000378:metabolism / Q000648:ultrastructure; D005260:Female; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D008854:Microscopy, Electron; D012964:Sodium / Q000378:metabolism*; D001743:Urinary Bladder / Q000502:physiology*; D014667:Vasopressins / Q000494:pharmacology*
D014667:Vasopressins; D000584:Amiloride; D012964:Sodium